The broad aim of this proposal is to examine how the CNS compensates for the loss of sensory and motor inputs during the production of postural reactions. In order to reveal the control signals involved in compensatory adaptation, response modulation over time must be examined. It is hypothesized that when sensory or motor function is impaired, postural behaviors become more constrained and response options decrease. Reduced control options may be sufficient in a constrained environment that requires a limited repertoire of response behaviors. In a complex environment with multiple signals, however, responses may not be adaptive to stimulus context. Specifically, adaptive modifications between the head, neck, and trunk during random and predictable linear translations in healthy subjects and in those with labyrinthine loss and cerebellar damage while seated in the dark with and without the trunk constrained will be examined. Response kinematics (head and trunk angular velocity and muscle activations) will be analyzed with overlapping windows of Fast Fourier Transforms to examine the time-frequency behavior. Center of pressure and center of mass will be calculated to estimate effective stiffness and damping characteristics of the adaptation process. The head will be weighted or the neck stiffened to investigate how an inertial field modifies the time- frequency behaviors. Statistical analyses will determine whether a damaged CNS exhibits the same rate of adaptation to these changes. We will quantify these control parameters using a recursive nonlinear system identification of incremental stiffness and damping matrices. Physiological control variables will be predicted using the homeomorphic computational model of the head and neck developed in this lab. Using a virtual environment, the contribution of dynamic visual inputs to the time varying adaptation process and the relative influence of a dynamic visual field on the head-neck-trunk responses will also be examined. It is hypothesized that patients with labyrinthine loss will select a single control strategy of increasing stiffness, thereby interfering with the coordinative process between the head and trunk. Patients with cerebellar lesions will be unable to modulate so that their responses are either excessive or suppressed. The functional consequences of labyrinthine loss and cerebellar control on postural orientation and stability are not well defined. Quantification of the adaptation process should reveal its effectiveness in a natural, dynamic environment and may suggest methods for remediation of postural instability.